[Studies on the "transmission" of Masugi nephritis in rats. X. Transmission by lymphocytes from lymphatic vessel drainage].
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to E F Pfeiffer.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
In the history of diabetes research, surgically induced experimental diabetes is usually associated with the names of Minkowski and von Mering on the basis of their investigations in 1889. However, temporary diabetes mellitus had already been induced 200 years previously by Johann Conrad Brunner (1653-1727) in an experiment in dogs. According to present-day knowledge, this temporary diabetes mellitus must be ascribed to subtotal pancreatectomy and reversible traumatic damage to the remaining endocrine pancreas. The brilliant experimenter Brunner did not associate the symptoms he produced with diabetes. Diabetes research would possibly have taken a different course had he done so.
The common denominator of the numerous data collected from experimental studies on isolated organs, on healthy subjects and on diabetic patients, is a specific effect of sulfonylureas on insulin release in the presence (or absence) of glucose. However, there are significant differences in the capacity of the various chemical preparations active in that respect. There are biochemical data suggesting that the glyburide- and chlorpropamide-type of preparations are affecting sites of the B-cells that are different from both the glucose and the tolbutamide receptors. Thus, glibenclamide seems to be qualitatively different from the older sulfonylureas, being more a potentiator than a stimulator. Therefore, we called this type the representative of 'the second generation' drugs. The extra-B-cell actions of these drugs, predominantly the stimulation of somatostatin and the inhibition of glucagon, are favorably adding to these antidiabetic actions. In clinical therapy, these specific properties make it possible to diagnose and to treat patients successfully who were regarded before as being non-responsive to sulfonylureas and being insulin-dependent. On the basis of blood glucose decreases and C-peptide increases, a specific glibenclamide-glucose-response-test has been described which is a valuable medium for predicting the outcome of oral antidiabetic therapy.